The oiginal concept is evaluated stressing that zinc stabilizes biomembranes and tissue reactivity. The mechanisms of the effect were studied. It was demonstrated that zinc is an integral part of various biomembranes being present mostly in a certain macromolecular fraction of the membrane. The linkage of zinc to this component is very stable resisting lipid peroxidative deterioration of the membrane structure. It was also shown that zinc inhibits lipid peroxidation by inhibiting competitively NADPH-oxidase which is linked to lipid peroxidation. Zinc, however, inhibits other enzymes (ATPase) which regulate the function of membranes (in this experience the function being immobilization of macrophages) by high zinc diet. These cells don't migrate and phagocytose. Preliminary data are presented showing the interference of zinc with complement system - specifically with C-3 convertase. The final goal of our broad approach to the biology and pharmacology of zinc is to test and form a scientific basis for using zinc with pharmacological modality in the control of tissue injury.